Autoimmune diseases are characterized by attack of the immune system of an individual against its own tissues. Autoimmune diseases usually result from breakdown of tolerance of the immune system to its own antigens. The specific antigens recognized by the immune system in the various autoimmune diseases can be present systematically or they can be organ specific. For example, systemic lupus erthematosus (SLE) is characterized by the presence of autoantibodies to DNA, ribonucleoproteins, histones, and other molecules that are not organ specific. Other autoimmune diseases are characterized by the destruction of mostly one organ. Such autoimmune diseases include type I diabetes, in which the insulin producing .beta. cells of the islets of Langerhans in the pancreas are destroyed.
In some autoimmune diseases, tissue destruction occurs primarily as a result of the production of high levels of autoantibodies. Such diseases include rheumatoid arthritis, characterized by destruction of the joint cartilage and inflammation of the synovium. Patients with rheumatoid arthritis have an accumulation of immune complexes in their joints which are formed by association of autoantibodies against the Fc portion of IgG and IgG molecules. These immune complexes activate the complement cascade which results in tissue damage. Myasthenia gravis, a disease of progressive muscle weakness, is caused by the production of autoantibodies reactive to acetylcholine receptors in the motor end plates of neuromuscular junctions.
In other autoimmune diseases, tissue destruction does not appear to be primarily mediated by production of autoantibodies, but rather by auto-reactive T lymphocytes. For example, experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis, and characterized by demyelination in the brain and the spinal cord, can be induced in naive animals by transfer of CD4+ T cells from diseased animals. Thus, it is generally considered that EAE represents a T cell mediated autoimmune disease, rather than a B cell mediated autoimmune disease (Ben-Nun, A. et al. (1981) Eur. J. Immunol., 11, 195).
Multiple sclerosis (MS) is a common demyclinating disease of the brain and spinal cord. It is a progressive disease that is characterized by remissions and exacerbations of neurologic dysfunction affecting different regions of the central nervous system. The symptoms of the disease result from a focus of inflammatory demyelination, which later forms a scar, appearing as a "plaque" in the white matter of the brain, brain stem or spinal cord. Presently, there is no definitive diagnostic test available for MS and diagnoses and treatment regimes are being formulated based on such factors as the extent of a patient's symptoms and/or the age of the patient at the time of onset of the exacerbations of neurologic dysfunction.
Patients having MS typically have been treated with steroids with a goal of either sending the patient into remission or slowing the progression of the disease in the patient. Other drugs have been used to treat particular symptoms of the disease, e.g. muscle relaxants. Recent developments in treatments available for MS include the administration of beta-interferon. Beta interferon has shown some promise for slowing the progression of the disease. However, effective treatments for MS are still needed.